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Do you have more detail on that? I've followed the TimeMoldSlimeMold "chemical hunger" theory and most of its in-detail critiques, and I don't remember one disputing the existence of the "Lipostat".
I also predisposed from personal anecdotes to strongly believe in the Lipostat, since I'm fit and very active, but also never have gained a single kilo during the long periods of sports injuries I've suffered through in the past.
Sure, there are a variety of feedback mechanisms, mostly neuropeptides of various flavors, that are involved with the production and regulation of appetite. As someone with a control theory background (hence the name), it's extremely easy to observe something that kinda looks like a feedback mechanism and then just jump all the way to, "THERE MUST BE A EQUILIBRIUM POINT NEGATIVE FEEDBACK CONTROLLER THAT TRACKS A KNOWN REFERENCE POINT!" It's extremely easy to imagine that such a thing is going on. It's vastly more difficult to understand how all the differing systems interact to produce some sort of global behavior.
For a simple example, suppose there is some subsystem that is doing a pretty decent job of doing closed-loop stabilization of a reference equilibrium point. Where does it get that reference from? Well, it's some other biological system, for sure. But which one? How? Does it interact with the environment? Culture? What? Things start to get tricky. What properties does it have? The most ardent supporters will make claims like, "Once you gain weight, it changes your reference point, and so your body 'fights' to defend it (I.e., the lower-level closed loop controller tracks the new reference point)." This is obviously plausible, but then it inspires equally obvious follow-on questions. What happens when you lose weight? Does this again change the reference point, so your body 'fights' to keep the lower weight? Most advocates will disagree. They will say things like that it's 'inevitable' that you will regain that weight, because your body is always and forever still tracking a higher reference point. What is the mechanism involved in this one-way ratchet? Ehhhhh... nobody knows?
Aside: I've also done some neuroscience-related work. Feedback pathways are complicated. Even the ones that seem like they might look simple at first. Even the ones where we can isolate specific neurons involved in what appears to be an extremely local system in simpler animals (various peptide interaction pathways are more complicated). They can be highly state-dependent; they can be highly nonlinear; they can produce oscillatory or bifurcation behavior. Anyway.
So, we could go out and try to set up some studies. Purely observational studies at the level of behavior are super challenging. You basically have just a bunch of different time series for weight. These are, frankly, going to look all sorts of different. Incredibly so if you're just taking a completely hands-off approach, just letting people do what they're going to do in life, but just weigh them on whatever interval. You'll have essentially no ability to say much of anything. So one route you could go is to try to induce a change in the hypothesized 'set point'. Maybe you make some group of folks lose weight; maybe you make another set of folks gain weight; maybe you have some maintain. Then, you let them loose and see what happens after some time. Folks are going to move around, and it's not necessarily going to be correlated. Oh by the way, what did you choose as your sample population? Did you start with obese people and have them lose weight? Or start with lean people and have them gain weight? Huge possible selection bias involved that you're going to have to somehow tease out. How do you go about doing so? Tease out environmental factors? Cultural?
Maybe, hopefully, you can also take some more invasive measurements to get at things like peptide levels, but they're swimming in a vat of all sorts of stuff going on in there, and you're kind of poking around in the dark. It's incredibly difficult to get at something along the lines of, "When you gain weight, it causes an increase in production of peptide X generally, and then losing weight again doesn't reduce such production," especially in a way that teases out a variety of other possible contributors. We've been pretty lucky to be able to see various features of a more direct intervention, like GLP-1 agonists, with regards to a few systems as a whole, but the work so far hasn't really firmed up any more general theory about 'set points'.
Interestingly, because of doubly labeled water measurements, we're actually able to do a lot more on the calories out side of the process. We have pretty good equations that do a pretty good job of estimation, at the population level, how many calories a body uses, as a function of things like fat-free mass, activity level, etc. They're obviously not perfect, and not perfect at the individual level, but they do a pretty good job. They've even told us that people do have some amount of hysteresis after gaining weight, but the dynamics (especially long-term) are about as clear as mud. But that doesn't help us on the side that most people care a lot about, which is calories in.
In the end, if you have basically no idea how the hypothesized 'set point' is getting 'set' (or getting changed), it calls into question the entire model of whether you actually are dealing with a decoupled set of systems, where one system is simply creating a 'set point' and another system is tracking it. Why do you think you have such strong decoupling? How can you demonstrate that such decoupling exists? Maybe they've actually been coupled systems all along. Maybe that coupling is weak; maybe that coupling is strong. You don't know a priori. I've seen all sorts of control theory inspired attempts at explaining all sorts of biological behavior (very different from weight regulation) in all sorts of animal models. Some are more convincing than others, and you always have in the back of your mind the question, "Are we imposing too much structure at a high-level to what is, inside, an incredibly complicated, time-dependent, state-dependent, nonlinear process?" There are a few cases where we have good theoretical reasons to think we can get away with it. See, for example, nonlinear averaging theory with applications to insect flight. But even there, we have it pretty well on the scale of tens-to-hundreds of wing beats, and we start to run into these thorny problems as soon as we try to loop in an higher-level system that includes, for example, visual observation of the environment. We can get some glimpses in some cases, but they really are sort of a case-by-case for how believable the experimental work is.
In the end, I would say that various forms of set point theory are, indeed, plausible at some level. There are huge theoretical and experimental hurdles to overcome in order to verify that it's what's actually going on. Anecdotes aren't the best guide. And even if some form of set point theory works, it mostly pushes the question back a level to how the set point is being set, be it due to inherent biological processes, environment, culture, etc. Perhaps it is some form of contaminant or something; I'm not saying that that idea is wrong. I'm saying that we have to do some hard work to isolate out different possibilities in order to know, first, what the "something" is that is being rejected, understand what the evidence is for rejecting it, and then why the only things left in the "something else" category are things like contaminants. I think SMTM is extremely casual in rejecting everything else and that to spell out the argument in detail shows how many steps were skipped. You really really can't jump directly from, "It appears that perhaps there are some feedback loops operating at some levels," all the way to, "Therefore, it must be a contaminant," in a single bound.
Very interesting, thank's for that detailed reply! I assumed by default that biological systems are full of such feedback loops, however complicated they may be in real life. Is the water equally as muddy for core temperature, blood sugar, testosterone level, serotonin, dopamine? I assume the first two are understood well, and testosterone starts being muddy?
I haven't really looked into all the different areas, so unfortunately, I probably shouldn't conclude much. Even with core temp, which seems like the easiest for likely simplifications, I'm not sure if we have much work to identify and quantify a mechanism for the colloquial sense of things like, "So and so grew up in Climate X, and when they moved to Climate Y, they always felt hot/cold for years until they adapted in some way." But again, that's mostly my ignorance.
For blood sugar/testosterone, I think we have a pretty good ability to 'tap in' to the inputs/outputs in simplified form that makes some sense. But there are some complicated feedback pathways that affect those sources/sinks, especially in the long-term, and I don't really know the state-of-the-art. Mostly just from what I've read from Scott on serotonin/dopamine, there's a lot of mud there.
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